It is known that the blood pressure of surgery patients falls from a pre-anaesthetic induction level to a lower level during induction of sedation/anaesthesia. This reduction in blood pressure has to be corrected by the anaesthetist to at least a level that is likely to reliably support the patient's vital functions.
The drop in blood pressure through the anaesthetic induction phase is widely viewed as being the result of a fall in systemic vascular resistance (SVR; SVR=[((mean arterial pressure−central venous pressure)*80)/cardiac output)]; the unit normally used for expressing SVR is dynes*s*cm-5) due to the administered anaesthetic drug(s) causing a vasodilatory response of the arterial tree. The arteries and pre-capillary arterioles provide about two thirds of the resistance to flow in the vascular system. Arterial vasodilation increases arterial capacity and consequently reduces the affected vasculature's resistance to blood flow. As the mean arterial pressure (MAP) is the product of cardiac output (CO) and systemic vascular resistance (MAP=CO*SVR), a reduction in SVR brings about a corresponding blood pressure reduction if the cardiac output remains the same.
While a fall in blood pressure can be caused by arterial vasodilation and the above discussed associated decrease in systemic vascular resistance, a number of other factors also influence blood pressure. Changes in cardiac output can also affect blood pressure/MAP. Cardiac output (expressed in l/min) is the product of stroke volume (SV, expressed in ml) and heart rate (HR, expressed in bpm). A fall in heart rate will therefore reduce cardiac output and arterial blood pressure.
Cardiac stroke volume in turn is affected by a number of factors. One of these factors is the extent to which the left ventricle is filled before contraction. This factor is often referred to as preload. In the healthy heart the fuller the ventricle is before systole (contraction) the more that the ejected stroke volume will increase—up to a limit, as can be seen from the Frank Starling curve. The dependence of the filling of the left ventricle on the efficient venous return of blood to the right side of the heart is often referred to as preload dependence. If the venous blood flow to the heart is insufficient to adequately fill the left ventricle prior to its contraction, then the stroke volume is reduced.
The major collecting veins contain 64% of the total circulating blood volume. The diameter and tone of the major collection veins is adjusted through hormonal/neural effects on the vein's smooth muscle component. Drugs may influence the major collection veins' tone and capacitance. Dilation of the major collection veins and/or blood loss will reduce preload and consequently also stroke volume.
Another factor affecting blood pressure is the resistance to the ejection of blood from the left ventricle across the aortic valve into the systemic arterial circulation. This resistance can be considered the sum of all forces opposing ventricular muscle shortening. This factor is often referred to as afterload and is regularly (and incorrectly) considered to be the same/similar to systemic vascular resistance (SVR). A simple example can show that afterload and SVR are in fact not the same. If two patients with equal ventricular dimensions are considered, wherein the first patient has a MAP of 60 mmHg and a cardiac output of 4 l/min and the second patient has a MAP of 120 mmHg and a cardiac output of 8 l/min. Both of these patients will have the same SVR. The resistance to the ejection of blood from the left ventricle, however, differs by a factor of two, as is evident from the difference in MAP.
If the left ventricle is working in a preload dependent fashion then the ventricular internal fibre load applied during systole does not compromise the stroke volume ejected. In this case the patient's hemodynamic performance is deemed afterload independent. However, increases in afterload are poorly tolerated in patients with no preload reserve (at the top of Frank Starling curve, that is patients that could be fluid overloaded) and/or those patients with left ventricular systolic dysfunction.
Blood pressure is moreover affected by the heart's contractility. The term ‘contractility’ refers to the inotropic state of the left ventricular myocardium, that is the force and velocity with which the myocardial fibres contract with each heart beat. In clinical practice a variety of contraction-phase indices/parameters such as the velocity of fibre shortening, peak rate of ventricular pressure rise and the end-systolic pressure to volume relationship are in use. The inotropic state of the left ventricle can be changed/supported by the administration of an inotropic drug such as adrenaline. Low contractility and high afterload will reduce stroke volume.
U.S. Pat. No. 6,071,244 and US patent application US 2009/0131805, the entireties of which are herein incorporated by this reference, disclose hemodynamic monitors for determining stroke volume based on arterial blood pressure measurements.
The positive pressure in the thoracic cavity of patients on a respirator can affect the stroke volume of the patient's heart. US patent application US 2009/0131805 discloses that the necessary variations in this pressure can cause considerable variations of stroke volume over a respiratory cycle. US 2009/0131805 recognises that this is particularly the case for hypovolemic patients and proposes to use the degree of variation in stroke volume over a respiratory cycle as an indication of the hemodynamic status.
A major limitation in displaying parameters on screen in a clinical environment, in particular in operating theatres is that the space available for any kind of display is severely limited. At the same time, however, the display has to be fashioned so that the displayed information can be intuitively understood, even if the observer is not close to the display.